ArticleParasitology research2024
The cyclophilin D (CypD) of Toxoplasma gondii is involved in the parasite's response to oxidative stress damage.
Article in Parasitology research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- A non-catalytic interaction surface mediates recognition of spliceosomal factors by the Toxoplasma gondii cyclophilin TgCyp23.The Biochemical journal · 2026Article
- Structural and Kinetic Variability of Pathogen Cyclophilins: Functional Diversification and Therapeutic Potential.ACS infectious diseases · 2026Review
- Cyclophilins as key players in protozoan parasite infections.Parasites & vectors · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
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Abstract
The mitochondrial permeability transition pore (mPTP) significantly impacts mitochondrial responses to cell death signals through its structural opening. Cyclophilin D (CypD) serves as a key regulator of the mPTP and plays a pivotal role in governing mitochondrial responses to cell death. In this study, we have demonstrated that Toxoplasma expresses a homolog of cyclophilin D, named TgCypD, which is localized in the mitochondria. Depletion of TgCypD resulted in a modest inhibition of tachyzoite invasion and proliferation, with no notable effect on mitochondrial morphology. However, TgCypD deficiency led to the inhibition of cytochrome c release from mitochondria into the cytosol, thereby imparting resistance to oxidative stress-induced cell death. Our findings suggest that T. gondii contains the mPTP component protein TgCypD, which is intricately involved in regulating mitochondrial responses to cell death.
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Registered trials
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